The protective effect of losartan in the nephropathy of the diabetic rat includes the control of monoamine oxidase type A activity

Manni, Maria Elena; Bigagli, Elisabetta; Lodovici, Maura; Zazzeri, Marina; Raimondi, Laura

doi:10.1016/j.phrs.2011.11.010

Cited by 18 publications

(17 citation statements)

References 26 publications

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“…Clorgyline is an inhibitor of MAO activity and at the dose used in the present investigation it does not interfere with mouse behavior (Manni et al, 2012a(Manni et al, , 2012b(Manni et al, , 2013. T1AM pro-learning and hyperlagesic effects were not evident in the presence of clorgyline (Manni et al, 2013) and we now report that under these conditions, brain T1AM and TA1 levels did not increase, but rather decreased.…”

Section: Discussionmentioning

confidence: 86%

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In the brain of mice, 3-iodothyronamine (T1AM) is converted into 3-iodothyroacetic acid (TA1) and it is included within the signaling network connecting thyroid hormone metabolites with histamine

Laurino

Siena

Chiellini

et al. 2015

European Journal of Pharmacology

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Section: Discussionmentioning

confidence: 86%

“…Accordingly, modification of amine oxidases activities in thyroid neoplasies (Masini-Repiso 24), diabetes (Manni et al 2012b)and hypertension have been reported (Pino et al, 1997).…”

Section: Discussionmentioning

confidence: 99%

In the brain of mice, 3-iodothyronamine (T1AM) is converted into 3-iodothyroacetic acid (TA1) and it is included within the signaling network connecting thyroid hormone metabolites with histamine

Laurino

Siena

Chiellini

et al. 2015

European Journal of Pharmacology

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“…Moreover, clorgyline pretreatment also increased the systemic bioavailability of T1AM given i.c.v. (Manni et al ., ,). These findings suggested that generation of TA1 by deamination might contribute, at least in part, to the acute effects of T1AM in vivo and showed that oxidative deamination had a marked effect on T1AM pharmacokinetics Overall, it can be hypothesized that T1AM, TA1, and possibly TA0, should be considered as part of the large family of thyroid hormone metabolites with potential biological activity.…”

Section: Introductionmentioning

confidence: 99%

Histamine mediates behavioural and metabolic effects of 3‐iodothyroacetic acid, an endogenous end product of thyroid hormone metabolism

Musilli

Siena

Manni

et al. 2014

British J Pharmacology

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BACKGROUND AND PURPOSE3-Iodothyroacetic acid (TA1) is an end product of thyroid hormone metabolism. So far, it is not known if TA1 is present in mouse brain and if it has any pharmacological effects. EXPERIMENTAL APPROACHTA1 levels in mouse brain were measured by HPLC coupled to mass spectrometry. After i.c.v. administration of exogenous TA1 (0.4, 1.32 and 4 μg·kg −1 ) to mice, memory acquisition-retention (passive avoidance paradigm with a light-dark box), pain threshold to thermal stimulus (51.5°C; hot plate test) and plasma glucose (glucorefractometer) were evaluated. Similar assays were performed in mice pretreated with s.c. injections of the histamine H1 receptor antagonist pyrilamine (10 mg·kg ) and the corresponding WT strain. KEY RESULTSTA1 was found in the brain of CD1 but not of HDC mice. Exogenous TA1 induced amnesia (at 0.4 μg·kg ). All these effects were modulated by pyrilamine and zolantidine. In HDC −/− mice, TA1 (1.32 and 4 μg·kg −1) did not increase plasma glucose or induce hyperalgesia. CONCLUSIONS AND IMPLICATIONSBehavioural and metabolic effects of TA1 disclosed interactions between the thyroid and histaminergic systems. AbbreviationsT3, tri-iodothyronine; TA1, 3-iodothyroacetic acid; TA1M, 3-iodothyronamine; TRIAC, tri-iodothyroacetic acid

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“…When Losartan was administrated to the high-salt diet rats, the up-regulation of RAS in renal cortex especially in proximal tubules were reduced even though the blood pressure was not lowed, indicating that intrarenal RAS was not the only pivotal mechanism for high-diet induced hypertension. The 20mg/kg/day of Losartan is a usual dosage[24,25], but the other dosages such as 10mg/kg/day[26], 100mg/500ml in drinking water[27], 30mg/kg/day[28] and so on, are also adopted by researchers. So, in the present study, the dosage of Losartan may be not sufficient to this type hypertension.…”

Section: Discussionmentioning

confidence: 99%

Up-Regulation of Intrarenal Renin-Agiotensin System Contributes to Renal Damage in High-Salt Induced Hypertension Rats

Liang

Zheng

et al. 2014

Kidney Blood Press Res

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Background/Aims: To investigate the change of intrarenal renin-agiotensin system (RAS) and its role in high-salt induced hypertension. Methods: Wistar rats were divided into normal-salt (NS), high-salt diet (HS) and high-salt diet with Losartan group (HS+L), for 6 weeks. Systolic blood pressure (SBP) was monitored. Blood and urine samples were collected every 2 weeks. Angiotensinogen (AGT) was measured by ELISA. AGT mRNA and protein were measured by real-time PCR and immunohistochemistry. Renin activity and angiotensin II (Ang II) were measured by radioimmunoassay. Results: HS versus NS group, SBP increased from 2^nd week (P<0.05), urinary protein increased at 6^th week (P<0.05). Although plasma renin, AGT and Ang II had no significant changes (P>0.05), renal cortex renin, AGT, and Ang II increased significantly in HS (P<0.05). In HS+L, Losartan failed to reduce SBP (P>0.05) but abolished the increase of proteinuria (P<0.01), renal cortex renin, AGT, Ang II and urinary AGT reduced (P<0.05) while plasma renin, AGT and Ang II enhanced (P<0.05) when compared with HS. Urinary AGT was positively correlated with renal AGT (r=0.592, P <0.01) and Ang II (r=0.726, P <0.01). Conclusion: Inappropriate response of the renal RAS to a high salt diet may contribute to hypertension and renal damage, and urinary AGT could reflect intrarenal RAS activity.

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The protective effect of losartan in the nephropathy of the diabetic rat includes the control of monoamine oxidase type A activity

Cited by 18 publications

References 26 publications

In the brain of mice, 3-iodothyronamine (T1AM) is converted into 3-iodothyroacetic acid (TA1) and it is included within the signaling network connecting thyroid hormone metabolites with histamine

In the brain of mice, 3-iodothyronamine (T1AM) is converted into 3-iodothyroacetic acid (TA1) and it is included within the signaling network connecting thyroid hormone metabolites with histamine

Histamine mediates behavioural and metabolic effects of 3‐iodothyroacetic acid, an endogenous end product of thyroid hormone metabolism

Up-Regulation of Intrarenal Renin-Agiotensin System Contributes to Renal Damage in High-Salt Induced Hypertension Rats

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